ArticleGenome biology2020
Computational inference of cancer-specific vulnerabilities in clinical samples.
Article in Genome biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Bioinformatics approaches to analyzing CRISPR screen data: from dropout screens to single-cell CRISPR screens.Quantitative biology (Beijing, China) · 2022Article
- Aberrant Transcript Usage Is Associated with Homologous Recombination Deficiency and Predicts Therapeutic Response.Cancer research · 2022Article
- Gene essentiality for tumour growth influences neoantigen-directed immunoediting.Clinical and translational medicine · 2022Article
- SynLeGG: analysis and visualization of multiomics data for discovery of cancer 'Achilles Heels' and gene function relationships.Nucleic acids research · 2021Article
- In Silico Inference of Synthetic Cytotoxic Interactions from Paclitaxel Responses.International journal of molecular sciences · 2021Article
- Computational inference of cancer-specific vulnerabilities in clinical samples.Genome biology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystematic in vitro loss-of-function screens provide valuable resources that can facilitate the discovery of drugs targeting cancer vulnerabilities.
resultsWe develop a deep learning-based method to predict tumor-specific vulnerabilities in patient samples by leveraging a wealth of in vitro screening data. Acquired dependencies of tumors are inferred in cases in which one allele is disrupted by inactivating mutations or in association with oncogenic mutations. Nucleocytoplasmic transport by Ran GTPase is identified as a common vulnerability in Her2-positive breast cancers. Vulnerability to loss of Ku70/80 is predicted for tumors that are defective in homologous recombination and rely on nonhomologous end joining for DNA repair. Our experimental validation for Ran, Ku70/80, and a proteasome subunit using patient-derived cells shows that they can be targeted specifically in particular tumors that are predicted to be dependent on them.
conclusionThis approach can be applied to facilitate the development of precision therapeutic targets for different tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.